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There is an idiom called "prescribe the right medicine to the symptoms", which means that the doctor takes medicine for the patient's illness
.
The disease here is not a different type of disease, but the cause of the disease
.
There are many different types of neuropsychiatric diseases, and the pathogenesis is also complicated
.
If different diseases have the same mechanism behind it, can drugs be developed for this mechanism to apply to various diseases? The thalamus is generally regarded as a transfer station for sensory information.
More and more studies have shown that specific thalamic nuclei also play a certain role in the formation of learning and memory
.
The prothalamic nucleus, located in the front of the thalamus, has long been ignored in previous studies because of the lack of specific and effective manipulation methods.
Its behavioral functions, especially whether it participates in learning and memory and the pathogenesis of neuropsychiatric diseases, are not clear
.
On June 30, 2021, the team of Professor Feng Guoping from the Massachusetts Institute of Technology published an article on Neuron entitled Anterior Thalamic Dysfunction Underlies Cognitive Deficits in a Subset of Neuropsychiatric Disease Models, which is the first detailed study of the identification of the prothalamic nucleus.
It also reveals that the nucleus is involved in the pathogenesis of autism and schizophrenia at the same time
.
Dr.
Dheeraj Roy and Dr.
Ying Zhang are the co-first authors of the research paper
.
Through novel loop manipulation techniques and methods of transgenic mice, the researchers specifically manipulated the adjacent subregions of the prothalamic nucleus—the dorsal region of the prothalamic nucleus (AD) or the ventral region of the prothalamic nucleus (AV) and found that AD reduces the spatial learning ability of mice, and inhibiting AV affects mice's discrimination of specific spaces
.
To give a simple example, you once went to the wild and fell into a hunter's trap.
As a result, you will detour through that area in the future
.
Abnormal AD function will make you never remember the environment at that time, so you can still sway in the same area
.
The damage to the function of the AV will make you feel that the entire forest is a crime scene, so you are trembling like walking on thin ice (of course, the premise of this example is that you escaped from the hunter for the first time)
.
Dr.
Dheeraj Roy said: “These experiments show that two adjacent prothalamic nuclei can regulate the different processes of memory formation.
What’s more interesting is that these two adjacent prothalamic nuclei can perform their respective functions by projecting to the same cortical brain area.
This is beyond our expectations
.
"So does the prothalamic nucleus participate in the pathogenesis of neuropsychiatric diseases? Feng Guoping's team has long been committed to the study of neurological diseases such as autism.
Previous studies have found that the autism susceptibility gene Ptchd1 is selectively expressed in the thalamic reticular nucleus (TRN)
.
Specifically knocking out Ptchd1 in TRN, mice showed attention deficit and hyperactivity behavior
.
However, unlike patients with Ptchd1 mutations, the learning ability of these mice is normal, suggesting that Ptchd1 may affect learning and cognition through other brain regions
.
In this study, the researchers found that Ptchd1 is specifically and highly expressed in AD
.
Interestingly, through the screening of autism susceptibility genes, about a quarter of them are highly expressed in AD
.
Cognitive impairment is also the main symptom of schizophrenia, and a large number of schizophrenia susceptibility genes are also expressed specifically in AD
.
Next, they used CRISPR-Cas9 technology to inhibit the expression of the Ptchd1 gene in the mouse thalamus AD, and observed that the animals had memory impairment
.
Not only Ptchd1, the researchers conducted the same experiment on another gene related to autism and three genes related to schizophrenia, and saw similar results in all mice: after reducing the expression of these genes , Will cause memory impairment
.
The researchers further discovered that the knockout of these disease-causing genes will cause excessive excitement of AD neurons
.
The enhancement of synaptic connections between neurons is believed to be the basis of learning and memory
.
"When an animal is learning, the excitability of neurons increases, which increases the connections between neurons
.
But if the neurons are already over-excited at the baseline state, then they cannot be further enhanced during the learning process, thereby affecting the synapses.
Plasticity affects the learning and memory process", explained Dr.
Zhang Ying
.
Interestingly, the researchers found that different disease-causing genes cause neuronal hyperexcitability by regulating different ion channels, leading to abnormal neural circuits and changes in mouse behavior
.
Based on the above mechanism, researchers used chemical genetics to artificially reduce the excitability of AD neurons, so that the cognitive ability of knockout mice with different pathogenic genes returned to normal
.
Although the chemical genetic method has not yet been approved for use in humans, the researchers believe that this research provides a direction for other targeted therapies
.
"There are many genetic and environmental factors that may cause specific diseases, but in the final analysis, these factors must cause certain types of neuronal changes and affect related neural circuits before specific behaviors can occur.
.
"Professor Feng Guoping said, "From a therapeutic point of view, in this case, we may not track single molecules, because they may vary from person to person and are only related to a small number of patients; however, in the future At the upper cell level or circuit level, patients have more common characteristics
.
"Professor Feng Guoping said that this study reveals a new loop mechanism that regulates cognitive impairment, and also suggests that in the future development of new treatment methods, patients can be treated through biological pathogenesis rather than through different diseases.
Group treatment
.
Original link: https://doi.
org/10.
1016/j.
neuron.
2021.
06.
005 Plate maker: Notice for reprinting on the eleventh [Non-original article] The copyright of this article belongs to the author of the article, personal forwarding and sharing are welcome, without permission Reprinting is prohibited, the author has all legal rights, offenders must be investigated
.
.
The disease here is not a different type of disease, but the cause of the disease
.
There are many different types of neuropsychiatric diseases, and the pathogenesis is also complicated
.
If different diseases have the same mechanism behind it, can drugs be developed for this mechanism to apply to various diseases? The thalamus is generally regarded as a transfer station for sensory information.
More and more studies have shown that specific thalamic nuclei also play a certain role in the formation of learning and memory
.
The prothalamic nucleus, located in the front of the thalamus, has long been ignored in previous studies because of the lack of specific and effective manipulation methods.
Its behavioral functions, especially whether it participates in learning and memory and the pathogenesis of neuropsychiatric diseases, are not clear
.
On June 30, 2021, the team of Professor Feng Guoping from the Massachusetts Institute of Technology published an article on Neuron entitled Anterior Thalamic Dysfunction Underlies Cognitive Deficits in a Subset of Neuropsychiatric Disease Models, which is the first detailed study of the identification of the prothalamic nucleus.
It also reveals that the nucleus is involved in the pathogenesis of autism and schizophrenia at the same time
.
Dr.
Dheeraj Roy and Dr.
Ying Zhang are the co-first authors of the research paper
.
Through novel loop manipulation techniques and methods of transgenic mice, the researchers specifically manipulated the adjacent subregions of the prothalamic nucleus—the dorsal region of the prothalamic nucleus (AD) or the ventral region of the prothalamic nucleus (AV) and found that AD reduces the spatial learning ability of mice, and inhibiting AV affects mice's discrimination of specific spaces
.
To give a simple example, you once went to the wild and fell into a hunter's trap.
As a result, you will detour through that area in the future
.
Abnormal AD function will make you never remember the environment at that time, so you can still sway in the same area
.
The damage to the function of the AV will make you feel that the entire forest is a crime scene, so you are trembling like walking on thin ice (of course, the premise of this example is that you escaped from the hunter for the first time)
.
Dr.
Dheeraj Roy said: “These experiments show that two adjacent prothalamic nuclei can regulate the different processes of memory formation.
What’s more interesting is that these two adjacent prothalamic nuclei can perform their respective functions by projecting to the same cortical brain area.
This is beyond our expectations
.
"So does the prothalamic nucleus participate in the pathogenesis of neuropsychiatric diseases? Feng Guoping's team has long been committed to the study of neurological diseases such as autism.
Previous studies have found that the autism susceptibility gene Ptchd1 is selectively expressed in the thalamic reticular nucleus (TRN)
.
Specifically knocking out Ptchd1 in TRN, mice showed attention deficit and hyperactivity behavior
.
However, unlike patients with Ptchd1 mutations, the learning ability of these mice is normal, suggesting that Ptchd1 may affect learning and cognition through other brain regions
.
In this study, the researchers found that Ptchd1 is specifically and highly expressed in AD
.
Interestingly, through the screening of autism susceptibility genes, about a quarter of them are highly expressed in AD
.
Cognitive impairment is also the main symptom of schizophrenia, and a large number of schizophrenia susceptibility genes are also expressed specifically in AD
.
Next, they used CRISPR-Cas9 technology to inhibit the expression of the Ptchd1 gene in the mouse thalamus AD, and observed that the animals had memory impairment
.
Not only Ptchd1, the researchers conducted the same experiment on another gene related to autism and three genes related to schizophrenia, and saw similar results in all mice: after reducing the expression of these genes , Will cause memory impairment
.
The researchers further discovered that the knockout of these disease-causing genes will cause excessive excitement of AD neurons
.
The enhancement of synaptic connections between neurons is believed to be the basis of learning and memory
.
"When an animal is learning, the excitability of neurons increases, which increases the connections between neurons
.
But if the neurons are already over-excited at the baseline state, then they cannot be further enhanced during the learning process, thereby affecting the synapses.
Plasticity affects the learning and memory process", explained Dr.
Zhang Ying
.
Interestingly, the researchers found that different disease-causing genes cause neuronal hyperexcitability by regulating different ion channels, leading to abnormal neural circuits and changes in mouse behavior
.
Based on the above mechanism, researchers used chemical genetics to artificially reduce the excitability of AD neurons, so that the cognitive ability of knockout mice with different pathogenic genes returned to normal
.
Although the chemical genetic method has not yet been approved for use in humans, the researchers believe that this research provides a direction for other targeted therapies
.
"There are many genetic and environmental factors that may cause specific diseases, but in the final analysis, these factors must cause certain types of neuronal changes and affect related neural circuits before specific behaviors can occur.
.
"Professor Feng Guoping said, "From a therapeutic point of view, in this case, we may not track single molecules, because they may vary from person to person and are only related to a small number of patients; however, in the future At the upper cell level or circuit level, patients have more common characteristics
.
"Professor Feng Guoping said that this study reveals a new loop mechanism that regulates cognitive impairment, and also suggests that in the future development of new treatment methods, patients can be treated through biological pathogenesis rather than through different diseases.
Group treatment
.
Original link: https://doi.
org/10.
1016/j.
neuron.
2021.
06.
005 Plate maker: Notice for reprinting on the eleventh [Non-original article] The copyright of this article belongs to the author of the article, personal forwarding and sharing are welcome, without permission Reprinting is prohibited, the author has all legal rights, offenders must be investigated
.
